Derek Abbott graduated from the University of Virginia in 1993. He then matriculated to Vanderbilt University School of Medicine as an MSTP Student. While a graduate student, he studied the breast cancer genes BRCA1 and BRCA2, ultimately attaining a Ph.D. in Cell Biology. After completion of his medical school requirements, Dr. Abbott continued his clinical training in Anatomic Pathology at Brigham and Women's Hospital (Harvard Medical School) in Boston, MA. After completing his residency and board certification, Dr. Abbott joined the lab of Dr. Lewis Cantley in the Department of Systems biology at Harvard Medical School. While in Lew Cantley's lab, Dr. Abbott began deciphering the signal transduction cascade initiated by bacterial activation of the Crohn's Disease susceptibility protein, NOD2.

Dr. Abbott joined the Case Western Reserve University's Department of Pathology in the fall of 2006. He is currently the Arline and Curtis F. Garvin Professor of Medicine, a Professor of Pathology and the co-director of the CWRU Medical Scientist Training Program. Current interests in the lab include genotype:phenotype correlations in inflammatory disease, drug development in genetic inflammatory disease and synthetic biology approaches to translational medicine. Outside of lab, he's quite busy keeping up with his wife, Dr. Kathryn Teng – Service Line Director and the Division Chief of General Internal Medicine at MetroHealth and his two children, Annabelle and Nate.

Research Information

Research Interests

The last decade has seen an explosion in our ability to understand the genetics of disease. While we are able to generate genetic data in disease quickly, an important bottleneck lies in the understanding of genetic mutations’ role in disease. My lab utilizes cutting-edge cell editing technology, synthetic biology and chemical biology to understand mutations role in disease and to better understand key genetic nodal points for translational innovation. This approach has led to the discovery of novel inhibitors of the inflammatory disease kinase, RIPK2, and more recently to novel mechanisms to inhibit the pyroptotic pore protein, Gasdermin D. Both of these pharmaceutical intervention show efficacy in inflammatory diseases as diverse as Inflammatory Bowel Disease, Psoriasis, Sarcoidosis and Sepsis.